Azothemistry is the accumulation in the blood of nitrogenous metabolism products, usually of protein origin, usually caused by a violation of the excretory function of the kidneys.
Azothemis of any origin are characterized by:
- Decreasing the rate of filtration through the smallest structures of the kidneys - glomeruli;
- An increase in blood nitrogen of urea;
- Increased serum creatinine concentration;
- The index of the ratio of urea nitrogen to creatinine (normally the index value should not exceed 15).
Azothemistry may be prerenal, renal and postrenal.
Prerevalent azotemia arises due to disturbance of blood supply to the kidneys for any reason:
- Because of a decrease in the volume of circulating blood (in blood loss, with a strong dehydration of the organism, etc.);
- As a result of hemorrhage;
- With shock and development of heart failure.
At the same time, lowering the pressure in the vascular system leads to a reduction in glomerular filtration, so in the blood more and more accumulate products of nitrogen metabolism, increases creatinine.
Renal azotemia develops when the kidney parenchyma is damaged, most often it is acute glomerulonephritis, acute renal failure (for example, with damage to kidney tissues by nephrotoxic poisons, chemicals, toxins, etc.), acute tubular necrosis, etc.
At the same time, both nitrogen and creatinine are emitted, albeit much weaker, therefore, their ratio (index) remains normal or reduced, but the accumulation of nitrogenous products in the blood still increases.
At postrenal azotemia at the onset of the disease, the kidney function is not disturbed, but there is a mechanical obstruction of urine flow through the stone in the ureter, prostate tumor, bladder, compression of the ureter enlarged uterus, etc. This leads to the expansion of the cavity of the kidney, the development of hydronephrosis.
The index of urea nitrogen/creatinine increases (more than 15), as the reciprocal absorption of nitrogen in the glomeruli of the kidneys increases.
Basic manifestations of azotemia
Patients' well-being deteriorates as the azotemia grows and other symptoms of the underlying disease develop.
Sharply decreases diuresis (oliguria), even a possible cessation of urine excretion (anuria), patients are tormented with dry mouth and constant thirst, at the same time, significant edema, fluctuations in blood pressure.
Patients are pale, apathy, retarded, have a strong weakness, an accelerated heartbeat (tachycardia).
Treatment of azotemia
If treatment is initiated in a timely manner and it is adequately detected, then recovery may be possible, but delaying even with further intensive correction can still cause chronic renal failure.
Treatment, as a rule, includes:
- Obligatory elimination of the cause causing azotemia;
- The appointment of drugs that improve the functioning of the heart and normalize arterial pressure;
- Symptomatic therapy.